Hardison W G, Wood C A
Am J Physiol. 1978 Aug;235(2):E158-64. doi: 10.1152/ajpendo.1978.235.2.E158.
The bile salt independent fraction (BSIF) of canalicular bile flow from the isolated rat liver perfused with bicarbonate-free perfusate is 50% of that from the liver perfused with bicarbonate-containing perfusate. HCO3-excretion is nearly eliminated and Na+ and Cl- excretion is reduced 50%. Replacement of HCO3- into perfusate increased bile flow by 0.3 microliter/g.min without changing bile acid excretion rate. 5.5-Dimethyl-2,4-oxazolidinedione (DMO) produced a similar effect. DMO was passively distributed between bile and plasma. The data indicate that a bicarbonate transport mechanism is responsible for production of up to 50% of the BSIF. Another weak acid, N-5[5-(2-methoxyethoxy)-2-pyrimidinyl]sulfamoylbenzene (glymidine), was rapidly excreted into bile and increased bile flow by over 2.0 microliter/g.min. Glymidine is probably excreted by an independent organic anion transport mechanism, and any effect on the bicarbonate transport mechanism is obscured. Canaliculus-enriched hepatocyte membrane fractions contained no HCO3-stimulated ATPase activity. Either this enzyme is unimportant in hepatocyte bicarbonate transport or transport occurs across membranes other than the bile canalicular membrane.
用无碳酸氢盐灌流液灌注的离体大鼠肝脏，其胆小管胆汁流的胆盐非依赖部分（BSIF）是用含碳酸氢盐灌流液灌注肝脏的50%。HCO₃⁻分泌几乎消除，Na⁺和Cl⁻分泌减少50%。向灌流液中补充HCO₃⁻可使胆汁流量增加0.3微升/克·分钟，而胆汁酸排泄率不变。5,5 - 二甲基 - 2,4 - 恶唑烷二酮（DMO）产生了类似的效果。DMO在胆汁和血浆之间被动分布。数据表明，一种碳酸氢盐转运机制负责产生高达50%的BSIF。另一种弱酸N - 5[5 - (2 - 甲氧基乙氧基)-2 - 嘧啶基]氨磺酰苯（甘密定）迅速排泄到胆汁中，并使胆汁流量增加超过2.0微升/克·分钟。甘密定可能通过一种独立的有机阴离子转运机制排泄，对碳酸氢盐转运机制的任何影响都被掩盖了。富含胆小管的肝细胞膜部分没有HCO₃⁻刺激的ATP酶活性。要么这种酶在肝细胞碳酸氢盐转运中不重要，要么转运发生在除胆小管膜以外的其他膜上。
